Neural processing in the vertebrate spinal cord is critically dependent on neuromodulatory input from the brainstem, which is dominated by the monoamines serotonin (5HT) and norepinephrine (NE). In motoneurons, monoamines act via G-protein coupled pathways to facilitate a very large persistent inward current (PIC) that is generated primarily in the dendrites. This PIC dominates the motoneuron's electrical behavior, amplifying synaptic input as much as 5 to 10 fold and allowing generation of long lasting behaviors like plateau potentials. In essence, the cell is switched from a state of passive dendritic integration to having its behavior dominated by highly active dendrites. Monoaminergic input to the cord is very diffuse, affecting many motor pools simultaneously. This highly excitable state has been considered to be very stable. Does such a generalized state of high excitability cause widespread co-contraction? We propose instead that the net effect of monoaminergic input is to dramatically increase the sensitivity of motoneurons to a very specific input, the reciprocal inhibition evoked by antagonist muscle length changes. Because reciprocal inhibition suppresses the PIC, the degree to which dendrites integrate actively or passively becomes highly sensitive to joint rotation. As a result, the descending monoaminergic systems should promote not co-contraction but reciprocal movement patterns. All studies are carried out using voltage clamp techniques in an in vivo preparation with a natural level of brainstem monoaminergic input. In Aim 1, we consider what types of inhibition can control the PIC. Aim 2 focuses on how excitatory and inhibitory synaptic inputs interact in the control of the PIC. In Aims 3 and 4, we combine natural 3D movements of the hindlimb generated by a robotic arm with voltage clamp of motoneurons. This novel approach allows us to directly measure the coupling between muscle length and active dendritic integration via the PIC. The results will be directly relevant to spinal injury, in which monoaminergic input is severely disrupted. Drugs that mimic monoaminergic actions may restore the delicate balance required to control the interaction between movement and motoneuron electrical properties.